Evidence map›Paper›PMID 40402411›Full record

ReviewMolecular neurobiology2025

Glycation in Alzheimer's Disease and Type 2 Diabetes: The Prospect of Dual Drug Approaches for Therapeutic Interventions.

Sama Ayoub, Maryam Arabi, Yousef Al-Najjar, Ibrahim Laswi, Tiago F Outeiro, Ali Chaari

Abstract readReview
In one paragraph

Review in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Sama AyoubWeill Cornell Medicine-Qatar, Qatar Foundation, Education City, P.O. Box 24144, Doha, Qatar.
Maryam ArabiWeill Cornell Medicine-Qatar, Qatar Foundation, Education City, P.O. Box 24144, Doha, Qatar.
Yousef Al-NajjarWeill Cornell Medicine-Qatar, Qatar Foundation, Education City, P.O. Box 24144, Doha, Qatar.
Ibrahim LaswiDepartment of Internal Medicine, Yale New Haven Hospital, New Haven, CT, USA.
Tiago F OuteiroDepartment of Experimental Neurodegeneration, Center for Biostructural Imaging of Neurodegeneration, University Medical Center Göttingen, Göttingen, Germany.
Ali ChaariWeill Cornell Medicine-Qatar, Qatar Foundation, Education City, P.O. Box 24144, Doha, Qatar. alc2033@qatar-med.cornell.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As global life expectancy increases, the prevalence of neurodegenerative diseases like Alzheimer's disease (AD) continues to rise. Since therapeutic options are minimal, a deeper understanding of the pathophysiology is essential for improved diagnosis and treatments. AD is marked by the aggregation of Aβ proteins, tau hyperphosphorylation, and progressive neuronal loss, though its precise origins remain poorly understood. Meanwhile, type 2 diabetes mellitus (T2DM) is characterized by chronic hyperglycemia, leading to the formation of advanced glycation end products (AGEs), which are implicated in tissue damage and neurotoxicity. These AGEs can be resistant to proteolysis and, therefore, accumulate, exacerbating AD pathology and accelerating neurodegeneration. Insulin resistance, a hallmark of T2DM, further complicates AD pathogenesis by promoting tau hyperphosphorylation and Aβ plaque accumulation. Additionally, gut microbiome dysbiosis in T2DM fosters AGE accumulation and neuroinflammation, underscoring the intricate relationship between metabolic disorders, gut health, and neurodegenerative processes. This complex interplay presents both a challenge and a potential avenue for therapeutic intervention. Emerging evidence suggests that antidiabetic medications may offer cognitive benefits in AD, as well as in other neurodegenerative conditions, pointing to a shared pathophysiology. Thus, we posit that targeting AGEs, insulin signaling, and gut microbiota dynamics presents promising opportunities for innovative treatment approaches in AD and T2DM.

Indexed as

Alzheimer DiseaseDiabetes Mellitus, Type 2Glycation End Products, AdvancedHypoglycemic AgentsAnimalsGastrointestinal MicrobiomeHumansGlycation End Products, AdvancedHypoglycemic AgentsAdvanced glycation end products (AGEs)Alzheimer’s diseaseDual drugsType 2 diabetes

Identifiers

PMID40402411
PMCPMC12511161

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.